Long non-coding RNA RP11-84C13.1 promotes osteogenic differentiation of bone mesenchymal stem cells and alleviates osteoporosis progression via the miR-23b-3p/RUNX2 axis.

Abstract

The objective of the present study was to determine the role of RP11-84C13.1 in osteoporosis (OP) and its molecular mechanism. First, clinical samples were collected from OP patients and normal control patients. Human bone marrow stromal cells (hBMSCs) were extracted from femoral head tissues. Runt-related transcription factor 2 (RUNX2) and RP11-84C13.1 serum levels were assessed by reverse transcription-quantitative (RT-q)PCR. Following transfection of pcDNA-RP11-84C13.1, si-RP11-84C13.1, microRNA (miRNA)-23b-3p mimic and miRNA-23b-3p inhibitor, the expression levels of RUNX2 and RP11-84C13.1 were determined by RT-qPCR. In addition, the osteogenic ability of hBMSCs was assessed by Alizarin Red staining. The binding of RP11-84C13.1 to miRNA-23b-3p and the binding of miRNA-23b-3p to RUNX2 was confirmed by dual-luciferase reporter gene assay. Long non-coding RNA (lncRNA) RP11-84C13.1 was significantly downregulated in the serum of OP patients. The osteogenic differentiation-related genes RUNX2 and RP11-84C13.1 were markedly upregulated in a time-dependent manner, while the miRNA-23b-3p level gradually decreased in hBMSCs with the prolongation of osteogenesis. RP11-84C13.1 knockdown inhibited the osteogenic differentiation of hBMSCs. Furthermore, RP11-84C13.1 regulated RUNX2 expression by targeting miRNA-23b-3p. Overexpression of miRNA-23b-3p partially reversed the promoting effect of RP11-84C13.1 on the osteogenesis of hBMSCs. In conclusion, lncRNA RP11-84C13.1 upregulated RUNX2 by absorbing miRNA-23b-3p, and thus induced hBMSC osteogenesis to alleviate osteoporosis.